Title

Targeting Molecular Mechanism of Vascular Smooth Muscle Senescence Induced by Angiotensin II, A Potential Therapy via Senolytics and Senomorphics

Document Type

Article

Abstract

Cardiovascular disease (CVD) is a prevalent issue in the global aging population. Premature vascular aging such as elevated arterial stiffness appears to be a major risk factor for CVD. Vascular smooth muscle cells (VSMCs) are one of the essential parts of arterial pathology and prone to stress-induced senescence. The pervasiveness of senescent VSMCs in the vasculature increases with age and can be further expedited by various stressing events such as oxidative stress, mitochondria dysfunction, endoplasmic reticulum stress, and chronic inflammation. Angiotensin II (AngII) can induce many of these responses in VSMCs and is thus considered a key regulator of VSMC senescence associated with CVD. Understanding the precise mechanisms and consequences of senescent cell accumulation may uncover a new generation of therapies including senolytic and senomorphic compounds against CVD. Accordingly, in this review article, we discuss potential molecular mechanisms of VSMC senescence such as those induced by AngII and the therapeutic manipulations of senescence to control age-related CVD and associated conditions such as by senolytic.

Keywords

aging, angiotensin II, senolytic, vascular smooth muscle cells

Medical Subject Headings

Aging (physiology); Angiotensin II (physiology); Animals; Cardiovascular Diseases (prevention & control); Cellular Senescence; Humans; Molecular Targeted Therapy; Myocytes, Smooth Muscle (physiology); Renin-Angiotensin System

Publication Date

9-9-2020

Publication Title

International journal of molecular sciences

E-ISSN

1422-0067

Volume

21

Issue

18

PubMed ID

32916794

Digital Object Identifier (DOI)

10.3390/ijms21186579

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